Aims: The aim of this study was to investigate MacroH2A.1 immunoexpression
in tissues of sheep exposed to FE.
Background: The correlation between asbestiform fibers, lung cancer, pleural
mesothelioma, and other lung diseases is already well established as the
pathophisiological pathophysiological respiratory mechanisms involved by inhalation of
Fluoro-edenite (FE). The latter is represented by cell proliferation and inducing the
release of growth factors, cytokines, and reactive oxygen and nitrite species, with DNA
damage that causes chronic inflammation and carcinogenesis. MacroH2A.1, and histone
variant, seems to play a role in sensing the metabolic state of the cell and linking it with
chromatin. Physiologically, MacroH2A.1 is expressed at low levels in stem cells and it
became upregulated during differentiation, preventing reprogramming of induced
pluripotent stem cells and after nuclear transfer. In particular, MacroH2A.1 has been
shown to explicate a potent antitumor mechanism in vivo as it results upregulated in
senescent cells determining a permanent growth-arrest.
Objective: Evaluate the possible role of the histone variant in the organism in response
to deep insight understanding the mechanisms of toxicity and the cellular response to
Methods: Lung and lymph nodes of exposed sheep were selected. Samples were
processed for histological and immunihistochemical immunohistochemical evaluations.
Densitometric, morphometric, and statistical analysis analyses were conducted.
Results: Tissue sections of FE exposed sheep demonstrated overexpression of
MacroH2A.1 vs unexposed samples. The data suggest an involvement of these this
molecule in the cellular response triggered by FE directed exposure.
Conclusion: In this contest, MacroH2A.1 overexpression supports its function as an
epigenetic stabilizer that helps to establish and maintain differentiated states.